Soybeans are a major cash crop and investment commodity in North America and elsewhere. Soybean oil is one of the most widely used edible oils, and soybeans are used worldwide both in animal feed and in human food production.
Soybean sudden death syndrome (SDS) is a fungal disease of soybean (Glycine max (L.) Merr.), caused by Fusarium solani (Mart.) Sacc. f. sp. phaseoli (Burk.) Snyd. & Hans., type A (Rupe, 1989; Roy et al., 1989, O'Donnell and Gray, 1995). Since its discovery SDS has become one of the most destructive pests in soybean. It has been reported in nearly all states that soybean are grown, and it causes production problems in several states, being particularly destructive in Midwestern states. See generally (Mulrooney 1988, Gibson et al., 1994, Hartman et al., 1995, Wrather et al., 1995, 1996). For example, susceptible soybean cultivars had 5-60% lower yield than did resistant cultivars on F. solani infested sites in Illinois (Gibson et al., 1994).
Although the use of fungicides is effective in reducing the population level of the fungus, fungicide use is both uneconomical and environmentally unsound as a control measure in soybean production. Neither is crop rotation a practical means of fungal control since rotation with a non-susceptible crop for at least two years is necessary for reducing soybean losses. Therefore, it has long been felt by soybean breeders that use of resistant varieties is the most practical control measure.
Screening of soybean germplasm for resistance to SDS was begun soon after the discovery of the fungus in the U.S. (Gibson et al., 1994; Rupe et al., 1991). Soybean breeding for resistance to SDS has mostly utilized genes from the cultivar ‘Forrest’ (Hartwig 1970) and ‘Pyramid’ (Myers et al., 1980). However, low yield of these cultivars necessitates the introgression of their SDS resistance into elite germplasm with a minimum of linkage drag.
Resistance to SDS is multigenic and quantitative in soybean (Hnetkovsky et al., 1996; Njiti et al., 1996). Chang et al., (1996, 1997) estimated that Forrest has 5 genes required for resistance to SDS. Njiti et al., (1996) and Kilo et al., (1996) estimated that Pyramid has 3 genes required for resistance to SDS, 2 that were different from those in Forrest. The multiple genes and genetic backgrounds involved contribute to the difficulty breeders have in developing SDS resistant soybean varieties.
Breeding programs for SDS resistance rely primarily on field evaluations where fungal populations occur. However, these populations can be mixtures of undetermined amplitypes (Achenbach et al., 1996) and the environment can vary thereby affecting the overwintering and infection capability of the fungus. Although evaluations using single oospore based fungal isolates in controlled greenhouse environments are possible, they are prohibitively expensive and are difficult to manage for larger breeding programs. These deficiencies in each evaluation method made SDS a difficult trait for soybean improvement.
Genetic markers closely linked to important genes may be used to indirectly select for favorable alleles more efficiently than direct phenotypic selection (Lander and Thompson 1990). SDS resistance loci have been associated with RFLP and microsatellite markers and tentatively mapped to linkage groups G (two), N and C1 (from Forrest); to linkage group C2 (from Essex); to linkage groups A2, B and G (from Pyramid) (Hnetkovsky et al., 1996; Chang et al., 1996, 1997; Abu-Thredeih et al., 1996; Kilo et al., 1996; Torto et al., 1996). In addition SDS resistance loci have been associated with the SCN resistance phenotype (Gibson et al., 1994) and soybean cyst nematode (SCN) resistance loci rhg1, rhg3 and Rhg4 on linkage groups G, B, and A2 respectively (Webb et al., 1995; Chang et al., 1996, 1997; Abu-Thredeih et al., 1996; Kilo et al., 1996).
U.S. Pat. No. 5,491,081, issued to Webb with Assignee Pioneer HiBred International, Inc. describes a method for introgressing SCN resistance into soybean germplasm as well as quantitative trait loci associated with SCN. It also describes SCN as a particular problem to soybean breeders and farmers. However, this patent does not discuss soybean SDS.
Therefore, it is of particular importance, both to the soybean breeders and to farmers who grow and sell soybeans as a cash crop, to identify, through genetic mapping, the quantitative trait loci (QTL) for resistance to SDS, and to identify additional QTL for resistance to SCN. Knowing the QTLs associated with resistance to SDS and to SCN, soybean breeders will be better able to breed SDS resistant and SCN resistant soybean that also possess other genotypic and phenotypic characteristics required for commercial soybean lines.